The great sciatic nerve of the rabbit was sharply severed and immediately repaired by means either of nerve suture or nerve graft. The rate of axoplasmic flow, nerve conduction velocity, and chronaxie were measured two months after the operation, and the state of nerve regeneration was compared with respect to the methods of nerve repair.
The axoplasmic flow of the sensory nerve fibers favored perineurial suture, whereas the restoration of the nerve conduction velocity and the excitability of the motor nerve fibers was better, although not significantly, following epineurial suture, when a comparison was made between the methods of nerve suture. When nerve graft was compared with nerve suture, the axoplasmic flow and, to a lesser extent, the excitability were superior after the nerve graft. However, excellent recovery of the nerve conduction velocity was shown in the nerve suture.
Repair of peripheral nerve injury seems to be one of the surgical techniques in which the use of microsurgery is undoubtedly advantageous. From the present results, however, it seems unwarranted to think that the use of microsurgical techniques in peripheral nerve surgery necessarily leads to an improvement in operative results. Assessment of ultimate functional recovery of the peripheral nerves following microsurgical methods of nerve repair is presently of urgent importance.

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Epidural pressure and respiratory movement were simultaneously monitored in sixteen patients with various conditions such as brain tumor, hypertensive intracerebral hematoma, ruptured cerebral aneurysm and normal pressure hydrocephalus. Durations of the monitorings ranged from 12 to 233 hours, with an average of 5.2 days. In the majority of cases, higher levels of intracranial pressure were noticed during the night and early in the morning. Rapid variations of intracranial pressure appeared to some extent in all instances. Occurrence of the pressure waves were closely related to changes in respiratory movement, the latter being suppressed during the phase of pressure rise and activated in the phase of pressure fall.
Lundberg's A-waves were divided into two different patterns: typical A-waves with a stable plateau of pressure elevation like a trapezium and atypical A-waves with irregular fluctuations during rises of pressure, usually related to oscillatory changes in respiration. Typical A-waves appeared in both sleeping and waking stages of patients with brain tumors. This type of A-wave showed a tendency of rhythmical repetition when it appeared. On the other hand, atypical A-waves occurred prominently during the sleeping stage and their occurrence was predominant in patients with cerebrovascular accidents. Concerning the levels of rising pressure, atypical A-waves started from a relatively low base pressure, mostly below 22 mmHg, compared to the rising pressure of typical A-waves which ranged between 15 and 66 mmHg.
B-waves appeared in close correlation with the periodic changes in respiratory movement and their occurrence was clearly predominant in the sleeping stage of the patients, showing a similarity to atypical A-waves. Such B-type waves appeared in wide base pressure ranges between 0 and 70 mmHg.
Interestingly, oscillatory B-waves were transformed into atypical A-waves, in some cases. These findings may indicate a common mechanism in the appearance of B-waves and atypical A-waves.

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The nature of plateau waves is still unclear. In this experimental study, a possible relationship between the development of plateau waves and the activity of sympathetic vasomotor nerves was investigated using an experimental model of plateau waves produced in cats. Efferent discharge from the renal nerve activity (RNA) was recorded as an indicator for the sympathetic vasomotor tone. Intracranial pressure (ICP), systemic blood pressure (BP), endtidal CO₂, cerebral blood flow (CBF), arterial blood gases, electroencephalograms (EEG) and somatosensory evoked potentials were monitored. Effects of hyperventilation and intravenous injection of mannitol on plateau waves were also studied.
Experimental obstructive hydrocephalus was produced by injecting kaolin (250 mg of hydrated aluminum silicate) into the cisterna magna. Four weeks after the injection of kaolin, the central canal of the lumbar spinal cord was obliterated with a ligature placed around the dura mater. After the ligation of the spinal cord, ICP gradually increased, reaching a level of 30-100 mmHg during a period of 2-14 hours. Then, a plateau wave, a spontaneous abrupt rise in ICP up to the level of 70-160 mmHg with a duration of 4-33 minutes, was observed in all five animals.
A decrease in RNA as well as in BP was observed corresponding to a rise in ICP at the initial phase of plateau waves.
CBF, amplitude of EEG and somatosensory evoked potentials decreased at the peak of the plateau waves. There were no significant changes in endtidal CO₂ and arterial pCO₂.
Plateau waves disappeared rapidly either by hyperventilation or mannitol administration.
It was concluded that a temporary decrease in the sympathetic vasomotor tone in situations of increased intracranial pressure may initiate the development of plateau waves and metabolic factors secondary to brain ischemia may play a role in their perpetuation.

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Prolonged vasospasm was produced in the feline basilar arteries by subarachnoid application of oxyhemoglobin, and sequential changes in vascular ultrastructure were observed.
Firstly, small cored vesicles in the vascular nerve endings were transformed, decreased in number and finally disappeared in the course of development of vasospasms induced by oxyhemoglobin.
Myonecrosis was observed from 1-2 hrs after subarachnoid application of oxyhemoglobin, but it was limited to a small number of smooth muscle cells. In the intercellular spaces among smooth muscle cells, vacuoles, vesicles and granules which might be the cell debris from myonecrosis were visualized from 1-2 hrs after subarachnoid application of oxyhemoglobin, and slowly increased in number, but they were also limited to small areas even 24 hrs after subarachnoid application of oxyhemoglobin.
On the other hand, intimal changes were characteristic, including intrusion of myointimal cells, vesicles and granules into the basement membrane-like substance of the tunica intima, detachment of endothelial cells from the basement membrane-like substance and invasion of blood-borne cells in several layers into the subendothelial gaps. They developed massively 24 hrs after subarachnoid application of oxyhemoglobin. Constriction of the arterial wall resulted in a reduction of the luminal size.
It was suggested that ultrastructural changes in feline basilar arteries after subarachnoid application of oxyhemoglobin might occur as a consequence of vasospasms. These organic changes, especially intimal ones, might occur irreversibly in the early stage of prolonged vasospasms and facilitate the arterial luminal narrowing. Therefore, it is most important in the prevention of prolonged vasospasms to remove by early operations the subarachnoid clots which contain abundant oxyhemoglobin.

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This experiment was performed to study the pathophysiology of cerebral infarctions produced by segmental embolization of the trunk of the middle cerebral artery (MCA) of dogs and effects of embolectomy 3 or 6 hours after embolization.
A silicone rubber cylinder was injected into the cerevical internal carotid artery and segmental occlusion of MCA was produced (embolization group). In a separate group microsurgical embolectomy was performed 3 (3 hour embolectomy group) or 6 hours (6 hour embolectomy group) after embolization.
The animals in the three groups were kept alive for 4 to 7 days and neurological deficits were evaluated according to Smith's neurological evaluation score. After macroscopic observation of the involved brain, the infarct volume was calculated by the average end area method.
Regional cerebral blood flow (rCBF) was measured in the cortex of the anterior sylvian gyrus and posterior sylvian gyrus and in the basal ganglia on the affected side by a hydrogen clearance method. Sensory evoked potential (SEP) was also recorded in response to contralateral median nerve stimulation. The measurements of rCBF and SEP were repeated at intervals of an hour for 6 hours after embolization in the embolization group and 3 hour embolectomy group.
In the embolization group the animals exhibited severe neurological deficits and the neurological evaluation score was 2.7±0.34 (mean±SE). Infarcts involved the lobus pyriformis, thalamus and caudate nucleus. These infarct volumes reached 4.6±0.5 (mean±SE) cm³. The rCBF decreased significantly in all measured regions. In the basal ganglia rCBF decreased most remarkably from the original value of 53.9±13.0 (mean±SD) ml/ 100 g/min to 21.5 ±8.9 ml/ 100 g/min 6 hours after embolization. The amplitude of SEP decreased progressively from the resting value of 100% to 53.0 ± 7.6 (mean±SE) % 3 hours after embolization.
In the 3 hour embolectomy group all animals were able to walk and the neurological evaluation score was 1.1 ± 0.45. The infarct volume was 1.1 ±0.47 cm³. The rCBF was restored to the original value in the three measured regions 1 hour after embolectomy. The amplitude of SEP increased from 87.8±4.3% one hour after embolization to 110-120% after embolectomy.
In the 6 hour embolectomy group five out of 10 dogs could walk but the other five dogs exhibited severe neurological deficits and the mean neurological evaluation score was 2.1 ± 0.44. The infarct volume was 2.9 ± 0.54 cm³ and seven out of 10 dogs demonstrated hemorrhagic infarction or intracerebral hematoma.
This study suggests that early restoration of the perforating arteries of MCA prevents deep cerebral infarction in this model. Development of ischemic brain edema seems to be the most severe risk factor in the prognosis in this embolectomy. Measurements of rCBF and SEP are beneficial for the evaluation of reversibility of the function after ischemia.

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Eleven cases of anaplastic gliomas with extraneural metastases are reported in this paper. All cases fulfilled Weiss' minimal criteria for confirmation of extraneural metastases of gliomas. The cases were analysed according to the mode of metastases such as the blood stream, ventriculoperitoneal shunt and lymphogeneous spread.
The group of metastases via the blood stream included one case of cerebral ependymoblastoma, one anaplastic astrocytoma, one glioblastoma and two medulloblastomas. Main metastatic sites of organs were the liver in four cases, bone in three, and the lungs in two. Two cases of dural invasion by glioma tissue were confirmed by operation and autopsy. Venous invasion by tumor cells was verified histologically in one case of medulloblastoma. Blood stream metastases must be taken into consideration in cases of dural invasion and/or venous invasion by tumor tissue.
Two cases of metastases via a ventriculoperitoneal shunt were observed in cases of fourth ventricle ependymoblastoma and pontine glioblastoma. Marked leptomeningeal dissemination was recognized at autopsy in both cases. The case of ependymoblastoma with distinct peritoneal metastases showed ascites 22 months after the ventriculoperitoneal shunt. Two small peritoneal metastatic deposits were found in a case of pontine glioblastoma. Metastases by the shunting procedure might occur in cases of gliomas with leptomeningeal dissemination.
The group of lymphogeneous metastasis included three cases of anaplastic astrocytomas and one case of glioblastoma. All of these cases were operated on more than twice and bone flaps were removed in the first or the following operations. Three out of four cases showed massive extracranial encroachment of growth directly through the bony defect. Metastases to cervical lymph nodes on the craniotomy side was the first manifestation of this mode of metastasis.

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Seven autopsied cases of anaplastic gliomas were examined histologically in correlation with CT findings scanned shortly before death.
Tumor cells were found to spread over almost all the heterogeneous and homogeneous low density areas in the CT scan. However, it was quite difficult to differentiate, by the absorption values, tumor tissue, tumor invading zone, anaplasia of tumor, coagulation necrosis or perifocal edema. High cellularity of tumor tissue had a tendency to show high absorption values in the plain scan. In one case, the tumor invaded diffusely almost the whole brain but the absorption values were “isodense”. There was no CT evidence to show the distribution of tumor cells.
Contrast enhancement corresponded well to vascular proliferation in the tumor tissue but not necessarily to cellularity or anaplasia of the tumors. Threre was no significant CE in the areas of highly malignant glioma where the vascularity was similar to that of the normal brain or showed only a slight proliferation. These findings suggest that the contrast enhancement in the CT scan could be explained by the vascular proliferation or angiogenetic activity of gliomas.
Sequential observation of contrast enhancement in four cases showed that the increment of coagulation necrosis corresponded to the decrement of contrast enhancement. However, viable tumor tissue was found to invade the extensive areas of low density where the degree of contrast enhancement diminished in the follow-up CT scan.

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Sixty-seven cases of brain abscess including 52 cases of surgically verified brain abscess were experienced in our clinic during the 18 years from 1960 to 1978. Relationships between operative methods and operative mortality and morbidity were analyzed. Twelve out of 52 surgical cases died, and the surgical mortality was 22.2%. Among different methods of surgical treatment, such as total primary excision, aspiration alone and secondary excision following aspiration, secondary excision following aspiration revealed the lowest mortality.
When the brain abscess did not become smaller and the capsule of the brain abscess did not become thicker in spite of repeated aspiration, the outcome was poor. As far as surgical mortality was concerned, aspiration alone appeared to be more favorable than other surgical methods.
There were significant improvements in the survival rate and quality of survival with brain abscess in the post-CT era.
The indication, methods and timing of surgical procedures on brain abscess were discussed with CT scan analysis.

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